ArticleBMC oral health2026
Therapeutic potential of low-dose rosiglitazone in periodontitis: attenuation of inflammation and bone loss through macrophage reprogramming.
Article in BMC oral health, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesThis study aimed to investigate the effects of different dosages of the peroxisome proliferator-activated receptor gamma (PPAR-γ) agonist rosiglitazone on macrophage polarization, the expression of related inflammatory factors, and alveolar bone loss in the periodontal tissues of rats with experimental periodontitis, thereby providing experimental evidence supporting the potential use of rosiglitazone as a therapeutic agent for periodontitis. MATERIALS AND
methodsForty rats were randomly assigned to four groups (n=10 per group): control group (C group), periodontitis group (P group), low-dose rosiglitazone treatment group (L group), and high-dose rosiglitazone treatment group (H group). After two weeks of rosiglitazone treatment via intraperitoneal injection, mandibles were scanned by micro-CT to quantify alveolar bone loss, with measurements of bone volume fraction (BV/TV), cemento-enamel junction to alveolar bone crest (CEJ-ABC) distance, and bone mineral density (BMD). Macrophages examined using immunofluorescence to quantify M1 and M2 proportions, and immunohistochemistry was performed to evaluate expression of IL-1β, IL-10 and osteoclast.
resultsBoth the L and H groups significantly reduced the M1/M2 macrophage ratio and IL-1β expression in periodontal tissues compared to the P group (p<0.001), with no statistically significant differences observed between L and H groups. The L group exhibited a marked increase in M2 macrophage population and IL-10 expression relative to both the P and H groups (p<0.001). The number of osteoclasts was significantly lower in both L and H groups compared to the P group (p<0.0001), though no significant difference was detected between the L and H regimens. These findings were consistent with the Micro-CT analysis of BV/TV and CEJ-ABC distance. Notably, the BMD in the L group was significantly higher than that in both P (p<0.0001) and H (p<0.05) groups.
conclusionBoth low- and high-dose rosiglitazone effectively attenuated alveolar bone loss and mitigated associated periodontal tissue inflammation in experimental periodontitis by modulating macrophage polarization and regulating inflammatory cytokine expression. Notably, low-dose rosiglitazone may offer superior benefits in promoting tissue repair during the advanced stages of periodontal inflammation. Clinical relevance: Rosiglitazone demonstrates promising potential as a therapeutic agent for the clinical management of periodontitis.Keywords Experimental periodontitis, Rosiglitazone, Macrophage polarization, PPAR, Periodontal therapy.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.